Roles of Hormones and Signaling Molecules in Describing the Relationship Between Obesity and Colon cancer

Sikalidis, Angelos K.; Varamini, Behzad

doi:10.1007/s12253-010-9352-9

Cited by 22 publications

(24 citation statements)

References 71 publications

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“…Although numerous adipokines have been identified, only a few have been extensively studied for their involvement in promoting or inhibiting colon cancer tumor growth. These include leptin, resistin, adiponectin, and others (38). Elevated levels of circulating leptin have been shown to increase the risk of colon cancer (37) and other malignancies.…”

Section: Adipose Tissue and Adipocytes In Obese Individuals Support Tmentioning

confidence: 99%

Putative Role of Adipose Tissue in Growth and Metabolism of Colon Cancer Cells

Schwartz

Yehuda‐Shnaidman

2014

Front. Oncol.

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Newly emerging data highlight obesity as an important risk factor for developing certain types of cancer, including colorectal cancer. Although evidence supports a link between the two, the mechanisms responsible for this relationship have not yet been fully elucidated. Hypertrophied and dysfunctional adipose tissue of the obese state is characterized by low-grade inflammation. Adipokines and cytokines secreted from adipocytes, together with the abundant availability of lipids from adipocytes in the tumor microenvironment, promote adhesion, migration, and invasion of tumor cells and support tumor progression and uncontrolled growth. One of the predisposed targets of the deleterious effects exerted by secretions from adipose tissue in obesity is the activities associated with the cellular mitochondria. Mitochondrial oxidative metabolism plays a key role in meeting cells’ energetic demands by oxidative phosphorylation (OxPhos). Here we discuss: (a) the dynamic relationship between glycolysis, the tricarboxylic acid cycle, and OxPhos; (b) the evidence for impaired OxPhos (i.e., mitochondrial dysfunction) in colon cancer; (c) the mechanisms by which mitochondrial dysfunction can predispose to cancer. We propose that impaired OxPhos increases susceptibility to colon cancer since OxPhos is sensitive to a large number of factors that are intrinsic to the host (e.g., inflammation). Given that adipocytes are a major source of adipokines and energy for the cancer cell, understanding the mechanisms of metabolic symbiosis between cancer cells and adipocytes should reveal new therapeutic possibilities.

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Section: Adipose Tissue and Adipocytes In Obese Individuals Support Tmentioning

confidence: 99%

Putative Role of Adipose Tissue in Growth and Metabolism of Colon Cancer Cells

Schwartz

Yehuda‐Shnaidman

2014

Front. Oncol.

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“…Even though the mechanisms remain not completely clarified, there is convincing evidence from epidemiological and experimental studies that dietary factors are likely to have a major influence on the risk of several types of cancer, particularly of the GI tract [93,94,95,96,97]. In vivo experiments using mice showed that diet-induced obesity increases risk of colonic cancer while a signaling/modular implication of leptin (both a hormone and a cytokine) was also suggested by the data [96,97].…”

Section: The Role Of Dietary Berries In Various Types Of Cancermentioning

confidence: 99%

Protective Role of Dietary Berries in Cancer

2016

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Dietary patterns, including regular consumption of particular foods such as berries as well as bioactive compounds, may confer specific molecular and cellular protection in addition to the overall epidemiologically observed benefits of plant food consumption (lower rates of obesity and chronic disease risk), further enhancing health. Mounting evidence reports a variety of health benefits of berry fruits that are usually attributed to their non-nutritive bioactive compounds, mainly phenolic substances such as flavonoids or anthocyanins. Although it is still unclear which particular constituents are responsible for the extended health benefits, it appears that whole berry consumption generally confers some anti-oxidant and anti-inflammatory protection to humans and animals. With regards to cancer, studies have reported beneficial effects of berries or their constituents including attenuation of inflammation, inhibition of angiogenesis, protection from DNA damage, as well as effects on apoptosis or proliferation rates of malignant cells. Berries extend effects on the proliferation rates of both premalignant and malignant cells. Their effect on premalignant cells is important for their ability to cause premalignant lesions to regress both in animals and in humans. The present review focuses primarily on in vivo and human dietary studies of various berry fruits and discusses whether regular dietary intake of berries can prevent cancer initiation and delay progression in humans or ameliorate patients’ cancer status.

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“…The loss of the sensitivity of cells to insulin is associated with changes in the signaling of chemokines, cytokines, growth hormones, and steroid hormones [88–90]. This may explain why metabolic disease goes along with an increased risk of certain cancers, for example, breast and colon cancer.…”

Section: Enzymes In the Sulfatase Pathway In Estrogen-associated Cmentioning

confidence: 99%

The Sulfatase Pathway for Estrogen Formation: Targets for the Treatment and Diagnosis of Hormone-Associated Tumors

Secky

Svoboda

Klameth

et al. 2013

Journal of Drug Delivery

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The extragonadal synthesis of biological active steroid hormones from their inactive precursors in target tissues is named “intracrinology.” Of particular importance for the progression of estrogen-dependent cancers is the in situ formation of the biological most active estrogen, 17beta-estradiol (E2). In cancer cells, conversion of inactive steroid hormone precursors to E2 is accomplished from inactive, sulfated estrogens in the “sulfatase pathway” and from androgens in the “aromatase pathway.” Here, we provide an overview about expression and function of enzymes of the “sulfatase pathway,” particularly steroid sulfatase (STS) that activates estrogens and estrogen sulfotransferase (SULT1E1) that converts active estrone (E1) and other estrogens to their inactive sulfates. High expression of STS and low expression of SULT1E1 will increase levels of active estrogens in malignant tumor cells leading to the stimulation of cell proliferation and cancer progression. Therefore, blocking the “sulfatase pathway” by STS inhibitors may offer an attractive strategy to reduce levels of active estrogens. STS inhibitors either applied in combination with aromatase inhibitors or as novel, dual aromatase-steroid sulfatase inhibiting drugs are currently under investigation. Furthermore, STS inhibitors are also suitable as enzyme–based cancer imaging agents applied in the biomedical imaging technique positron emission tomography (PET) for cancer diagnosis.

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Roles of Hormones and Signaling Molecules in Describing the Relationship Between Obesity and Colon cancer

Cited by 22 publications

References 71 publications

Putative Role of Adipose Tissue in Growth and Metabolism of Colon Cancer Cells

Putative Role of Adipose Tissue in Growth and Metabolism of Colon Cancer Cells

Protective Role of Dietary Berries in Cancer

The Sulfatase Pathway for Estrogen Formation: Targets for the Treatment and Diagnosis of Hormone-Associated Tumors

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